Antegrade selective cerebral perfusion with mild hypothermic systemic circulatory arrest during thoracic aortic surgery

Objective Antegrade selective cerebral perfusion (ASCP) and retrograde cerebral perfusion (RCP) have proven to be reliable methods of brain protection during aortic surgery. These techniques are usually accompanied by systemic circulatory arrest with moderate hypothermia (24–28°C) or deep hypothermia (18–24°C). However, hypothermia can lead to various problems. The present study therefore reports results for thoracic aorta replacement using ASCP with mild hypothermic systemic arrest (28–32°C).

Design Between 1995 and 2003, 68 consecutive patients underwent repair of the ascending aorta and/or aortic arch. Mild hypothermic ASCP was utilized in 31 cases, moderate hypothermic ASCP in 20, and deep hypothermic RCP in 17. Various parameters were compared between the mild hypothermic ASCP, moderate hypothermic ASCP, and RCP.

Results Hospital mortality was 10.3%, with no significant differences observed between any groups. Permanent neurological dysfunction was 8.8%, and no significant differences were observed between any groups. Mild hypothermic ASCP displayed significantly decreased transfusion volume, intubation time, and ICU stay.

Conclusions Use of ASCP with mild hypothermic systemic circulatory arrest during aortic surgery resulted in acceptable hospital mortality and neurological outcomes. ASCP with mild hypothermic arrest allows decreased transfusion volume and reduced duration of intubation and ICU stay.     

亚低温抑制重型颅脑创伤诱导Tau蛋白过度磷酸化的实验研究

目的 观察亚低温对重型颅脑创伤诱导的Tau蛋白磷酸化的影响.方法 体外研究通过细胞液压冲击仪建立SK-N-SH细胞损伤模型,观察冲击1h、6h和12h后Tau蛋白的磷酸化水平.体内研究通过小动物液压冲击仪建立大鼠重型颅脑损伤模型(2.4 atm),接受或不接受亚低温治疗(33℃,4h).观察液压冲击6h、24 h和72 h后Tau蛋白的磷酸化水平,以及亚低温对此变化的影响.结果 SK-N-SH细胞在液压冲击后,Tau蛋白在Thr231和Ser396位点的磷酸化水平从1h开始升高,到6h左右达到高峰.SD大鼠在液压冲击后,Tau蛋白在Thr231和Ser396位点的磷酸化水平从6h开始升高,到24h左右达到高峰,到72 h仍处于高水平;免疫组化的结果也显示,大鼠脑部海马CA1区和皮质区的Tau蛋白磷酸化水平在Thr231位点也明显增高.亚低温可显著逆转液压冲击诱导的SD大鼠Tau蛋白过度磷酸化(P＜0.01).结论 亚低温可抑制重型颅脑创伤诱导的Tau蛋白过度磷酸化.     

Therapeutic hypothermia and acute brain injury

Secondary brain injury has devastating effects on morbidity, mortality and good functional outcomes. Neuroprotection is multimodal, with decades of preclinical and small clinical studies showing the benefits of therapeutic hypothermia. The basic scientific principles have merit, yet large randomized controlled trials fail to show a clear benefit. This article will review the basic science – the practical aspects of delivering targeted temperature management and evaluate the evidence behind its use for acute brain injuries. With a lack of high-quality evidence for hypothermia, recent consensus statements are shifting the paradigm away from hypothermia to the maintenance of normothermia and prevention of pyrexia.     

亚低温治疗所致感染并发症的研究进展

亚低温治疗常用于脑、脊髓、心脏等器官的缺血性或外伤性损害,对这些器官有明显的保护作用,然而其在治疗过程中亦可诱发多种并发症。本文主要就亚低温治疗过程中感染并发症的发病机制、临床特点、诊断、防治及预后等方面作一综述。     

全身麻醉患儿术后恢复期保温措施研究

目的探讨非气管插管全身麻醉患儿术后转入麻醉恢复室的最佳保温方法。方法选择非气管插管全身麻醉手术后转入麻醉恢复室患儿120例,按随机数字表法分为S1组、S2组和C组各40例。S1组采用加温系统实施主动保温,温度调节为38℃;S2组采用加温毯实施主动保温,温度调节为38℃;C组采用常规盖棉被保暖。观察三组生命体征变化、意识恢复时间、在麻醉恢复室停留时间、低体温及并发症发生率的差异。结果三组不同时间体温和心率比较,干预效应、时间效应均P0.05,交互效应均P0.05。三组术后意识恢复时间、恢复室停留时间、低体温和寒战发生率比较,差异有统计学意义(P0.05,P0.01),S1组各项指标更优。结论对非气管插管全麻手术后患儿在麻醉恢复室实施加温系统主动保温,可以降低术后低体温发生率,有助于患儿尽快恢复。     

低温海水浸泡对大鼠血浆蛋白质组的影响研究

目的模拟海难落水所致重度低体温损伤,比较鉴定低温海水浸泡模型动物血浆蛋白质组差异,为研究低体温相关血浆蛋白提供线索。方法将50只雄性健康Wistar大鼠平均分成5组,分别在低温海水中浸泡0、2、4、6、10 h后采集下腔静脉血。分离血浆后,用试剂盒去除Ig G和白蛋白等高丰度蛋白,并经过除盐后采用蛋白质双向凝胶电泳(2-DE)分离。对差异1.5倍以上的蛋白斑点,用基质辅助激光解析电离飞行时间质谱(MALDI-TOF-MS)进行肽质量指纹图谱分析,应用NCBI或Swiss-prot数据库鉴定差异蛋白质。结果大鼠浸泡在15℃海水中,中心体温(肛温)迅速下降,浸泡30 min降至19℃,浸泡120 min降至16℃左右,体温维持不变,说明进入重度低体温状态。初步鉴定出3个与低温相关差异蛋白,肺表面相关蛋白A(SP-A)、丝氨酸蛋白酶抑制剂A3K(SPA3K)和抑制物组织基质金属蛋白酶抑制剂-3(TIMP-3)。与正常大鼠相比,这3个蛋白的表达水平均随着低温海水浸泡时间的延长明显上调。结论低温海水浸泡后的大鼠血浆蛋白质组相对正常大鼠血浆蛋白质组有改变。研究差异蛋白有助于阐明低温损伤的分子机制,为研究和治疗低体温症提供靶标。